title: Transcriptional repression by COUP-TF II is dependent on the C-terminal domain and involves the N-CoR variant, RIP13delta1.
abstract: COUP-TF II/ARP-1 is an 'orphan' steroid receptor that inhibits basal transcription, and represses trans-activation by the vitamin D, thyroid hormone and retinoid receptors. The molecular basis of repression by COUP-TF II remains obscure. In this study we utilized the GAL4 hybrid system to demonstrate that COUP-TF II contains sequences within the C-terminal region that encode a dominant transcriptional repressor that inhibits the ability of the potent chimeric transactivator GAL4VP16 to induce transcription. Mammalian two hybrid analysis demonstrated that COUP-TF II did not efficiently interact with either interaction domains I or II from N-CoR and RIP13. However, COUP-TF II efficiently interacts with a region comprised of interaction domains I + II from the corepressor, RIP13delta1. Efficient interaction of the orphan receptor with the corepressor was critically dependent on a large region comprised of the C, D and E domains of COUP-TF II, which correlated with the domain that maximally represses transcription. This investigation suggested that the N-CoR variant, RIP13delta1 interacts with a region of COUP-TF II that functions as a dominant transcriptional repressor.
authors.affiliation: University of Queensland, Centre for Molecular and Cellular Biology, Ritchie Research Laboratories, Brisbane, Australia.
authors.forename: P J
authors.initials: PJ
authors.lastname: Bailey
authors.forename: D H
authors.initials: DH
authors.lastname: Dowhan
authors.forename: K
authors.initials: K
authors.lastname: Franke
authors.forename: L J
authors.initials: LJ
authors.lastname: Burke
authors.forename: M
authors.initials: M
authors.lastname: Downes
authors.forename: G E
authors.initials: GE
authors.lastname: Muscat
mesh_terms: D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D019556:COS Cells; D051836:COUP Transcription Factors; D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics; D004268:DNA-Binding Proteins / Q000737:chemistry / Q000378:metabolism*; D005656:Fungal Proteins / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D019319:Okadaic Acid / Q000494:pharmacology; D011987:Receptors, Steroid; D015534:Trans-Activators / Q000378:metabolism; D014157:Transcription Factors / Q000737:chemistry / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects; D014407:Tumor Cells, Cultured
chemical_list: D051836:COUP Transcription Factors; D004268:DNA-Binding Proteins; D005656:Fungal Proteins; C070633:Gal-VP16; D011987:Receptors, Steroid; D015534:Trans-Activators; D014157:Transcription Factors; D019319:Okadaic Acid; D015124:8-Bromo Cyclic Adenosine Monophosphate; D015500:Chloramphenicol O-Acetyltransferase